Maternal and child health has been linked to the development of the human conceptus which absolutely depends on adequate and balanced supplies of key nutrients; therefore, an important element of reproductive health and neurodevelopment is improved nutritional status in women of child bearing age. Defect in neurodevelopment of newborn costs the mother both psychological and emotional stress, also reproductive health failure has been a significant public health concern, because it leads to disability in couples and individuals who bear the burden, there is therefore an urgent need to understand the underlying of birth malformation in order to channel possible solution. This study therefore sought to investigate the reproductive and neurodevelopmental defects in rat models of F
0 , F
1 and F
2 generations after modeled dietary protein deficiency, establishing the consequential mechanistic association. Rats in four groups were fed different ration of protein diet (PD); 21% PD, 10%PD, 5%PD and control diet (Normal rat chow), from adolescent through to gestation and Lactation, and next generations were weaned to the maternal diet group. Reproductive function and fertility index (including oestrus cyclicity, sexual response, histopathology and hormone profiling), as well as Neurobehavioral studies to include; Learning Memory tests (Y-maze, Moriz water maze, Elevated Plus Maze and Open field test) and Brain oxidative stress. Result shows significant reduction in the %fertility index and the overall reproductive function in the protein deficient models (5%PD; 35%2.5 10%PD; 66%2.2 as compared to 21%PD; 88.4%0.8, and control 85.8%1.3) which persist in subsequent generation. There was also observable transgenerational cognitive impairment reflected in: The Y-maze (Spatial memory: 5%; 8.3%, 10%; 9.25% 21%; 57.6% and control 55.95%), Morizz water Maze (5%: 26.5; 10%;21, 21%;5 and control; 6, as escape latency time), there was a significant decrease in the antioxidant capacity of the brain, especially in the 5%PD models. Brain serotonin and dopamine levels respectively; 5%: 2.70.3; 36.25 0.57., 10%; 2.90.3; 17.75 0.94., 21%;7.80.9; 7.951.1., and control; 70.2; 11.550.7. were significantly perturbed in the test model brains. Therefore, Protein deficiency is capable of causing a dysfunction in the reproductive health of models, by altering the oestrus cyclicity which is partly dependent on the changes in hormonal events, the brain redox status and neurotransmitter system. Therefore, persistent perinatal exposure to protein malnutrition increases the risk of cognitive defect and other brain disorders in subsequent generations. There was an evidence of metabolic reset in the malnourished group; this may be due in part to epigenetic regulation of transposable element.
Perinatal dietary protein deficiency perturbs neurodevelopment and cognitive behavior of F1 and F2-generations of rat models
